AHR-dependent misregulation of Wnt signaling disrupts tissue regeneration.
The origins of molecular toxicology can be traced to understanding the interactions between halogenated aromatic hydrocarbons and the aryl hydrocarbon receptor (AHR). The physiological consequences of activation of the aryl hydrocarbon receptor are diverse, and we are just beginning to understand the importance of the AHR signal transduction pathway in homeostasis and disease. The many downstream targets that mediate these biological responses remain undefined. Studies have exploited the power of the zebrafish model to elucidate the mechanisms by which AHR activation disrupts biological signaling. Recent genomic analysis performed in a zebrafish tissue regeneration model revealed functional cross talk between AHR and the well-established Wnt/beta-catenin signal transduction pathway. This review focuses on the development of the zebrafish model of AHR biology and the application of in vivo toxicogenomics to unravel molecular mechanisms.
Mathew
Lijoy K
LK
Department of Environmental & Molecular Toxicology, and the Environmental Health Sciences Center Oregon State University, Corvallis, OR 97331-7301, USA.
Simonich
Michel T
MT
Tanguay
Robert L
RL
D000818:Animals; D005121:Extremities / Q000502:physiology; D006801:Humans; D008954:Models, Biological; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity; D018336:Receptors, Aryl Hydrocarbon / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D012038:Regeneration / Q000235:genetics / Q000502:physiology*; D012098:Reproduction / Q000187:drug effects / Q000502:physiology; D015398:Signal Transduction; D051153:Wnt Proteins / Q000235:genetics / Q000378:metabolism*; D015027:Zebrafish / Q000235:genetics / Q000378:metabolism / Q000502:physiology
D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon; D051153:Wnt Proteins